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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

B-cell CLL/lymphoma 6

The protein encoded by this gene is a zinc finger transcription factor and contains an N-terminal POZ domain. This protein acts as a sequence-specific repressor of transcription, and has been shown to modulate the transcription of START-dependent IL-4 responses of B cells. This protein can interact with a variety of POZ-containing proteins that function as transcription corepressors. This gene is found to be frequently translocated and hypermutated in diffuse large-cell lymphoma (DLCL), and may be involved in the pathogenesis of DLCL. Alternatively spliced transcript variants encoding different protein isoforms have been found for this gene. [provided by RefSeq, Sep 2008] (from NCBI)
Top mentioned proteins: bcl-2, p27, MUM1, HAD, c-Myc
Papers using bcl-6 antibodies
Quantifying the role of aberrant somatic hypermutation in transformation of follicular lymphoma
Delabie Jan et al., In Journal of Hematopathology, 2007
... BCL-6 (PG-B6p)DAKO Cytomation, Denmark A/S ...
De novo CD5+ diffuse large B-cell lymphoma: a clinicopathologic study of 109 patients
Stein Harald et al., In Virchows Archiv, 2001
... BCL6594Citrate1:25Dako ...
Alterations of a zinc finger-encoding gene, BCL-6, in diffuse large-cell lymphoma
Joh T et al., In British Journal of Cancer, 1992
... We purchased the following antibodies: rabbit anti-BCL6 monoclonal antibody (EP529Y; Epitomics, Burlingame, CA, USA); rabbit ...
Papers on bcl-6
Subtype-specific addiction of the activated B-cell subset of diffuse large B-cell lymphoma to FOXP1.
Tucker et al., Austin, United States. In Proc Natl Acad Sci U S A, Feb 2016
FOXP1 promoted gene expression underlying transition of the GCB cell to the plasmablast-the transient B-cell stage targeted in ABC-DLBCL transformation-by antagonizing pathways distinctive of GCB-DLBCL, including that of the GCB "master regulator," BCL6 (B-cell lymphoma 6).
Intrafollicular Epstein-Barr virus-positive large B cell lymphoma. A variant of "germinotropic" lymphoproliferative disorder.
Facchetti et al., Brescia, Italy. In Virchows Arch, Feb 2016
Lymph nodes showed an effaced nodular architecture with abnormal B follicles colonized by EBV+ large, pleomorphic atypical cells, including Reed-Sternberg-like cells, showing an activated B cell phenotype (CD10-FOXP1-Bcl6-IRF4+ or CD10-FOXP1+Bcl6+IRF4+) and intense expression of CD30.
Malignant hematopoietic cell lines: in vitro models for double-hit B-cell lymphomas.
MacLeod et al., Braunschweig, Germany. In Leuk Lymphoma, Feb 2016
UNASSIGNED: Mature B-cell lymphomas with concurrent rearrangements of MYC and BCL2 (more rarely BCL6), "double-hit lymphomas" (DHLs), form a heterogeneous group.
The FOXO1 Transcription Factor Instructs the Germinal Center Dark Zone Program.
Dalla-Favera et al., New York City, United States. In Immunity, Jan 2016
The function of FOXO1 in sustaining the DZ program involved the trans-activation of the chemokine receptor CXCR4, and cooperation with the BCL6 transcription factor in the trans-repression of genes involved in immune activation, DNA repair, and plasma cell differentiation.
Double-hit and double-protein-expression lymphomas: aggressive and refractory lymphomas.
Coiffier et al., Lyon, France. In Lancet Oncol, Nov 2015
Over time, the definition was modified and now includes diffuse large B-cell lymphoma (DLBCL) with MYC translocation combined with an additional translocation involving BCL2 or BCL6.
A Novel Non-Immunoglobulin (non-Ig)/BCL6 Translocation in Diffuse Large B-Cell Lymphoma Involving Chromosome 10q11.21 Loci and Review on Clinical Consequences of BCL6 Rearrangements.
Papajik et al., Olomouc, Czech Republic. In Pathol Oncol Res, Sep 2015
UNASSIGNED: BCL6 rearrangements (3q27) are the most common chromosomal abnormalities in diffuse large B-cell lymphoma (DLBCL), with numerous immunoglobulin (Ig) and non-Ig genes as partners.
Consistent in-frame internal tandem duplications of BCOR characterize clear cell sarcoma of the kidney.
Kiyokawa et al., Tokyo, Japan. In Nat Genet, Aug 2015
We identified internal tandem duplications in the BCOR gene (BCL6 corepressor) affecting the C terminus in 100% (20/20) of CCSK tumors but in none (0/193) of the other pediatric renal tumors.
[Human herpesvirus 8-negative primary effusion lymphoma-like lymphoma with t(8;14)(q24;q32)].
Aiba et al., In Rinsho Ketsueki, Aug 2015
The pathological examination of the pleural effusion showed proliferation of atypical large lymphoid cells, which were positive for CD19, CD20, CD10, CD38, CD7, BCL2 and BCL6 but negative for CD5, CD30, MUM1, surface immunoglobulin, HHV-8 and EBV.
[Research Progress on TKI Resistance of CML Cells Mediated by MSC through CXCL12/CXCR4 Axis].
Li et al., Nanchang, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, Aug 2015
Studies recently have shown that the mesenchymal stem cells (MSC) can induce CML cells to resist TKI therapy by CXCL12/CXCR4 axis from multiple aspects, such as the directional migration of CML cells, adherence to marrow cavity, the mediation of cell protective dormancy, activations of numerous survival signaling pathways, the suppression of mitochondrial-dependent apoptosis and the up-regulated expression of BCL-6.
Self-enforcing feedback activation between BCL6 and pre-B cell receptor signaling defines a distinct subtype of acute lymphoblastic leukemia.
Müschen et al., San Francisco, United States. In Cancer Cell, Apr 2015
In these cases, tonic pre-BCR signaling induced activation of BCL6, which in turn increased pre-BCR signaling output at the transcriptional level.
A BCL6/BCOR/SIRT1 complex triggers neurogenesis and suppresses medulloblastoma by repressing Sonic Hedgehog signaling.
Vanderhaeghen et al., Brussels, Belgium. In Cancer Cell, 2015
Here we identify BCL6, a transcriptional repressor and lymphoma oncoprotein, as a pivotal factor required for neurogenesis and tumor suppression of medulloblastoma (MB).
The importance of B cell-T cell interaction in autoimmune diseases.
Tanaka et al., In Nihon Rinsho Meneki Gakkai Kaishi, 2014
We found that combination with BCR, CD40 and TLR9 or IL-4/IL-21 signal via tyrosine kinases such as Syk/Btk/JAK caused robust gene expression of AICDA, BCL6, XBP1 and IgG production.
Utility of immunohistochemistry with an antibody against MYC at the initial diagnosis of follicular lymphoma, grade 3A, for predicting a more aggressive clinical course: a case report and review of the literature.
Hirano et al., Tokyo, Japan. In Int J Clin Exp Pathol, 2014
Here, we present a FL patient who transformed to a B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt's lymphoma, accompanied by concurrent BCL2, BCL6, and MYC translocations; i.e., triple-hit lymphoma.
Nodal Marginal Zone Large B-Cell Lymphoma with Burkitt Translocation and Complex Chromosomal Changes Associated with Overexpression of BCL2, MYC, and BCL6.
Kuenstner et al., In J Clin Exp Hematop, 2014
Malignant B-cells were CD10 negative, harbored Burkitt translocation, and multiple chromosomal changes including trisomies of chromosomes 3 and 18, and three copies of 8q with an intact q24 cytoband (in addition to MYC rearrangement), associated with overexpression of BCL6, BCL2, and MYC respectively.
Cytogenetic Study and Analysis of Protein Expression in Plasma Cell Myeloma with t(11;14)(q13;q32): Absence of BCL6 and SOX11, and Infrequent Expression of CD20 and PAX5.
Miura et al., In J Clin Exp Hematop, 2014
Cyclin D1, CD38, and BCL2 were detected in all patients; on the other hand, neither BCL6 nor SOX11 was detected in any of the evaluated patients.
POZ-, AT-hook-, and zinc finger-containing protein (PATZ) interacts with human oncogene B cell lymphoma 6 (BCL6) and is required for its negative autoregulation.
Fedele et al., Napoli, Italy. In J Biol Chem, 2012
disruption of one or both Patz1 alleles may favor lymphomagenesis by activating the BCL6 pathway
Bcl6 and Maf cooperate to instruct human follicular helper CD4 T cell differentiation.
Crotty et al., Los Angeles, United States. In J Immunol, 2012
Bcl6 and Maf collaborate to orchestrate a suite of genes that define core characteristics of human Tfh cell biology.
PIM1 gene cooperates with human BCL6 gene to promote the development of lymphomas.
Baron et al., Chicago, United States. In Proc Natl Acad Sci U S A, 2012
Concurrent expression of BCL6 and PIM1 in lymphomas, is reported.
The Bcl6-SMRT/NCoR cistrome represses inflammation to attenuate atherosclerosis.
Evans et al., Los Angeles, United States. In Cell Metab, 2012
These results reveal that Bcl6-SMRT/NCoR complexes constrain immune responses and contribute to the prevention of atherosclerosis.
Increased frequency of circulating follicular helper T cells in patients with rheumatoid arthritis.
Wang et al., Zhenjiang, China. In Clin Dev Immunol, 2011
increased T cell gene expression in rheumatoid arthritis patients
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